Following Are Some Of the Most Commonly Used  Drugs Classes With Mechanism of actions

Beta Lactam Antibiotics:

Mostl Commonly Used Drugs In This Class Are Penicillin and Cephalosporins
This Is Not A Single Drug But A group Of Different Other Agents Which Includes :
Penicillin G, procaine penicillin, benzathine penicillin, penicillin V and many more
These Antibiotics Are Also Called “Cell Wall Synthesis Inhibitors”
Mostly Used Drugs Include :
1) Penicillin,
2) Cephalosporin,

Mechanism Of Penicillin:

Penicillin inhibits transpeptidase and preventing the remodeling of the peptidoglycan layer. These Transpeptidase Enzyme Is Responsible For The Linking Of Sub Units Of Amino Acid Which Is Responsible For The Cell Wall Synthesis.

2) Cephalosporin drugs are divided into different generations depending upon their microbial spectrum.
1.First generation:
Some Commonly Used drugs In This Class Are:
Cefadroxil
Cephalexin
Cefalotin
Cefazolin
Cefradine
Ceftezole

2.Second generation:
Following Are The Most Commonly Used Medications In This Group;
Cefaclor
Cefonicid
Cefprozil
Cefuroxime
Cefuzonam.

3.Third generation
Cefixime
Cefpodoxime
Cefatoxime
Cefdinir
Cefoperazone
ceftazidime
4.Fourth generation:
cefepime
5.Fifth generation:
Ceftaroline

Mechanism Of Action Of Cephalosporin:

Cephalosporins are bactericidal and have an indistinguishable method of activity from other β-lactam anti-infection agents, (for example, penicillins), yet are less helpless to β-lactamases. Cephalosporins disturb the union of the peptidoglycan layer shaping the bacterial cell divider. The peptidoglycan layer is vital for cell divider auxiliary respectability. The last transpeptidation venture in the combination of the peptidoglycan is encouraged by penicillin-binding proteins (PBPs). PBPs tie to the D-Ala-D-Ala toward the end of muropeptides (peptidoglycan precursors ) to crosslink the peptidoglycan. Beta-lactam antibiotics mimic the D-Ala-D-Ala site, along these lines irreversibly restraining PBP cross-linking of peptidoglycan.

Fluoroquinolones Antibiotics:

Mechanism of Action

Quinolones quickly restrain DNA union by advancing cleavage of bacterial DNA in the DNA-enzyme complexes of DNA gyrase and type IV topoisomerase, bringing about fast bacterial death.1–3 when in doubt, gram-negative bacterial action associates with hindrance of DNA gyrase, and gram-positive bacterial action compares with inhibition of DNA type IV topoisomerase 1
The Parent Compound Of This Class Of Antibiotics Is Nalidixic Acid.
Important And Most Commonly Drugs In This Class Are;
1)Norfloxacin
2)Ofloxacin
3)Ciprofloxacin
4)Levofloxacin
5)Gatifloxacin
6)Moxifloxacin
7)Trovafloxacin

High Blood Pressure (AntiHypertensive Drugs)

Angiotensin 2 Receptors Blockers

Mechanism:

Angiotensin II receptor blockers (ARBs) relax your veins, which brings down your pulse and makes it simpler for your heart to pump blood.
Angiotensin is a compound in your body that influences your cardiovascular framework in different ways, including narrowing your veins. This narrowing can expand your circulatory strain and compel your heart to work harder. Angiotensin II receptor blockers hinder the activity of angiotensin II, permitting veins to extend
Mostly Used Drugs In This Class Includes;
1)Valsartan
2)Losartan

Calcium Channel Blockers

Mechanism Of Action:

Inhibition of the flood of calcium through moderate directs in the vascular smooth muscles and myocardial tissue amid depolarization. This outcomes in systemic and coronary vein vasodilation, diminished myocardial contractility, and sinoatrial (SA) and atrioventricular (AV) nodal depression.
Most Commonly Used
1)Amlodipine

Beta blocker 

Beta blockers, otherwise called beta-adrenergic blocking agents, are medications that decrease your BP. Beta blockers work by obstructing the impacts of the hormone epinephrine, also known as called adrenaline. When you take beta blockers, your heart thumps all the more gradually and with less constrain, in this way lessening circulatory strain. Beta blockers likewise veins open up to enhance blood stream.
Mostly Used Drugs;
1)Carvedilol
2)Metoprolol
3)Atenolol

Alpha receptor agonist

1)Clonidine

Mechanism Of Clonidine

It stimulates the alpha 2 receptor of the vasomotor center of the brain,leading to decrease in the activity of sympathetic nerves to the peripheral tissues.inhibitiob of the sympathetic nerves to the blood vessels will cause vasodilation.both these effects will cause fall in blood bloodpressure.

Anticholesterol (Statins)

Mechanism Of Action:

Statins hinder an enzyme called HMG-CoA reductase, which controls cholesterol creation in the liver.
The medication obstructs the dynamic site of the compound, keeping different particles from actuating it, along these lines backing off the cholesterol generation handle.
Extra compounds in the liver cell sense that cholesterol generation has diminished and react by making a protein that prompts to an expansion in the creation of LDL (low-density lipoprotein, or “bad” cholesterol) receptors.
These receptors migrate to the liver cell films and tie to passing LDL and VLDL (very low-density lipoprotein)). The LDL and VLDL then enter the liver and are processed.
Individuals regularly start statin treatment to bring down their cholesterol level to beneath 5 millimoles per liter, or by 25-30 percent. The dose might be expanded if this objective does not come to. Treatment with statins more often than not proceeds even after the objective cholesterol level is come to proceed with the insurance against atherosclerosis.
Most Commonly Used Drugs
1)Atorvastatin
2)Lovastatin
3)Simastatin

Proton Pump Inhibitors

Mechanism:

The PPI ties irreversibly to a hydrogen/potassium ATPase catalyst (proton pump) on gastric parietal cells and obstructs the discharge of hydrogen particles, which consolidate with chloride particles in the stomach lumen to shape gastric acid.
Most Commonly Used Drugs:
1) Omeprazole
2)Esomeprazole
3)Lansoprazole

Antiseizure: (Anticonvulsion)

Mechanism Of Action:

1)Gabapentin
2)Pregabalin

Mechanism Of Gabapentin:

The exact Mechanism by which gabapentin delivers its pain relieving and antiepileptic activities are obscure(Unknown). Gabapentin is basically identified with the neurotransmitter gamma-aminobutyric corrosive (GABA) however has no impact on GABA official, take-up, or debasement. In vitro thinks about have demonstrated that gabapentin ties with high-fondness to the a2d subunit of voltage-enacted calcium channels; be that as it may, the relationship of this authoritative to the helpful impacts of gabapentin is obscure or unknown.

Antidiabetic drugs:

1)Metformin
2)Glyburide
3)Glibenclamide
4)Pioglitazone
5)Insulin

Mechanism of Action:

Sulphonylureas are settling on particular receptors and acts through the potassium channel from the pancreatic and the additional pancreatic level. At pancreatic level, increment insulin emission and at the level of pancreatic beta cells, they increase the quantity of insulin receptors. At additional pancreatic sulphonylurea drugs diminish hepatic gluconeogenesis (glucose union from non-sugar sources), expanded glycolysis and improves insulin activity in skeletal muscle and in fat tissue.

Aspirin

Mechanism Of Action:

The pain relieving, antipyretic, and calming impacts of acetylsalicylic corrosive are because of activities by both the acetyl and the salicylate parts of the in place atom and additionally by the dynamic salicylate metabolite. Acetylsalicylic corrosive specifically and irreversibly represses the action of both sorts of cyclooxygenase (COX-1 and COX-2) to diminish the development of antecedents of prostaglandins and thromboxanes from arachidonic corrosive. This makes acetylsalicylic corrosive unique in relation to different NSAIDS, (for example, diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may intensely repress prostaglandin development. Acetylsalicylic corrosive’s antirheumatic (nonsteroidal calming) activities are an aftereffect of its pain relieving and mitigating instruments; the helpful impacts are not because of pituitary-adrenal incitement. The platelet conglomeration hindering impact of acetylsalicylic Acid particularly includes the compound’s capacity to go about as an acetyl benefactor to cyclooxygenase; the nonacetylated salicylates have no clinically huge impact on platelet total. Irreversible acetylation renders cyclooxygenase idle, in this way keeping the arrangement of the totaling operator thromboxane A2 in platelets. Since platelets do not have the capacity to combine new proteins, the impacts persevere for the life of the uncovered platelets (7-10 days). Acetylsalicylic corrosive may likewise hinder creation of the platelet conglomeration inhibitor, prostacyclin (prostaglandin I2), by vein endothelial cells; in any case, restraint prostacyclin generation is not perpetual as endothelial cells can deliver more cyclooxygenase to supplant the non-practical catalyst.
Pain Medications:

Tramadol

Mechanism:

Tramadol and its O-desmethyl metabolite (M1) are specific, weak OP3-receptor agonists. opiate receptors are combined with G-protein receptors and capacity as both positive and negative controllers of synaptic transmission by means of G-proteins that initiate effector proteins. As the effector framework is adenylate cyclase and cAMP situated at the internal surface of the plasma film, opioids diminish intracellular cAMP by hindering adenylate cyclase. Along these lines, the arrival of nociceptive neurotransmitters, for example, substance P, GABA, dopamine, acetylcholine and noradrenaline is restrained. The pain relieving properties of Tramadol can be ascribed to norepinephrine and serotonin reuptake barricade in the CNS, which represses torment transmission in the spinal string. The (+) enantiomer has higher fondness for the OP3 receptor and specially represses serotonin take-up and upgrades serotonin discharge. The (- ) enantiomer specially hinders norepinephrine reuptake by fortifying alpha(2)- adrenergic receptors.

Acetaminophen

Mechanism:

Acetaminophen is thought to act essentially in the CNS, expanding the pain threshold by restraining both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 compounds required in prostaglandin (PG) amalgamation. Not at all like NSAIDs, acetaminophen does not restrain cyclooxygenase in fringe tissues and, hence, has no fringe calming influences. While headache medicine goes about as an irreversible inhibitor of COX and specifically hinders the chemical’s dynamic site, ponders have found that acetaminophen in a roundabout way pieces COX, and that this bar is insufficient within the sight of peroxides. This may clarify why acetaminophen is compelling in the focal sensory system and in endothelial cells however not in platelets and invulnerable cells which have abnormal amounts of peroxides. Ponders likewise report information proposing that acetaminophen specifically hinders a variation of the COX protein that is not the same as the known variations COX-1 and COX-2. This compound is currently alluded to as COX-3. Its correct system of activity is still ineffectively seen, yet future research may give assist knowledge into how it functions. The antipyretic properties of acetaminophen are likely because of direct impacts on the warmth controlling focuses of the hypothalamus bringing about fringe vasodilation, sweating and henceforth warm dispersal.